Our overall objective is to investigate the physiopharmacology of sympathetic neuro-effector junction and the afferent neuaral pathway involved in the production of experimental pulmonary hypertension. The following research objectives and specific aims are proposed: A) Assessment of the nature and extent to which sympathetic afferent nerves from the main pulmonary artery participate in the reflex production of experimental pulmonary hypertension. l) To determine the effects of bilateral transection of the sympathetic chain ganglia from Tl to T5 on the pulmonary hypertensive response to main pulmonary artery wall distention. 2) To record afferent discharges from the left cardiac nerve and/or the sympathetic ramus communications Tl-T5 before and during distention of the main pulmonary artery. B) Evaluation of the physiopharmacology of the efferent adrenergic neural-effector junction involved in the production of pulmonary hypertension. l) To determine the effects of norepinephrine stimulation of pulmonary vascular effectors before and after a) chemical blockade of alpha adrenergic receptors and b) chemical denervation of the adrenergic nervous system. 2) To determine the effects of dopamine stimulation of pulmonary vascular effectors before and after a) chemical blockade of alpha adrenergic receptors, b) chemical blockade of dopamine receptors and c) chemical denervation of the adrenergic nervous system. 3) To determine the effects of isoproterenol stimulation of pulmonary vascular effectors before and after chemical blockade of beta adrenergic receptors. 4) To correlate the presence and absence of sympathetic adrenergic nerves in the lung as demonstrated by catecholamine fluorescence techniques to the production of experimental pulmonary hypertension. 5) To determine the extent to which lung plasma catecholamine levels can be altered by distention of the pulmonary artery wall. 6) To compare the possible changes in lung plasma catecholamines produced by the pulmonary artery distention reflex to possible changes produced by stimulation of the stellate ganglion. 7) To determine the extent that lung catecholamine turnover rates are altered by distention of the pulmonary artery wall.